Absence of Alveolar Tears in Rat Lungs with Significant Alveolar Instability

• Published in: Respiration Vol. 74; no. 4; pp. 439 - 446
• Main Authors: Pavone, Lucio A., DiRocco, Joseph D., Carney, David E., Gatto, Louis A., McBride, Nils-Tomas D., Norton, Jillian A., Hession, Richard M., Boubert, Francoise, Hojnowski, Katy A., LaFollette, Ryan L., Dries, David J., Nieman, Gary F.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.01.2007; S. Karger AG
• Subjects: Animals; Biological and medical sciences; Disease Models, Animal; Hypotheses; Injuries; Injuries of the limb. Injuries of the spine; Interventional Pulmonology; Male; Medical sciences; Microscopy, Electron, Scanning; Microscopy, Video; Pneumology; Pulmonary Alveoli - injuries; Pulmonary Alveoli - ultrastructure; Pulmonary Gas Exchange - physiology; Rats; Rats, Sprague-Dawley; Respiration, Artificial - adverse effects; Respiratory diseases; Respiratory Distress Syndrome, Adult - etiology; Respiratory Distress Syndrome, Adult - pathology; Respiratory Distress Syndrome, Adult - physiopathology; Respiratory system : syndromes and miscellaneous diseases; Rodents; Rupture; Traumas. Diseases due to physical agents; Ventilation; Acute respiratory distress syndrome; Recruitment/derecruitment; Ventilator-induced lung injury; Microvascular fracture; Lung disease; Ventilator; Rat; Respiratory disease; Tear; Acute; Rodentia; Diseases of the osteoarticular system; Fracture; Trauma; Syndrome; Recruitment; Microcirculation; Vertebrata; Mammalia; Animal; Respiratory distress; Instability; Pneumology
• ISSN: 0025-7931; 1423-0356
• DOI: 10.1159/000101476

Background: Lung injury associated with the acute respiratory distress syndrome can be exacerbated by improper mechanical ventilation creating a secondary injury known as ventilator-induced lung injury (VILI). We hypothesized that VILI could be caused in part by alveolar recruitment/derecruitment resulting in gross tearing of the alveolus. Objectives: The exact mechanism of VILI has yet to be elucidated though multiple hypotheses have been proposed. In this study we tested the hypothesis that gross alveolar tearing plays a key role in the pathogenesis of VILI. Methods: Anesthetized rats were ventilated and instrumented for hemodynamic and blood gas measurements. Following baseline readings, rats were exposed to 90 min of either normal ventilation (control group: respiratory rate 35 min –1 , positive end-expiratory pressure 3 cm H 2 O, peak inflation pressure 14 cm H 2 O) or injurious ventilation (VILI group: respiratory rate 20 min –1 , positive end-expiratory pressure 0 cm H 2 O, peak inflation pressure 45 cm H 2 O). Parameters studied included hemodynamics, pulmonary variables, in vivovideo microscopy of alveolar mechanics (i.e. dynamic alveolar recruitment/derecruitment) and scanning electron microscopy to detect gross tears on the alveolar surface. Results: Injurious ventilation significantly increased alveolar instability after 45 min and alveoli remained unstable until the end of the study (electron microscopy after 90 min revealed that injurious ventilation did not cause gross tears in the alveolar surface). Conclusions: We demonstrated that alveolar instability induced by injurous ventilation does not cause gross alveolar tears, suggesting that the tissue injury in this animal VILI model is due to a mechanism other than gross rupture of the alveolus.